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This study was undertaken to verify the effects of GGH(1) on obesity using high fat diet induced male mice. Eight-week old C57BL/6N mice were used for all experiments. Standard chow diet fed mice were used as lean control and high fat diet induced obese mice were randomly divided into 4 groups : obese control, GGH(1)-125mg/kg, GGH(1)-250mg/kg and GGH(1)-500mg/kg. After mice were treated with oral administration for 8 weeks, body weight, feeding efficiency ratio, plasma triglyceride level and visceral adipose tissue weights were measured. Compared with obese controls, GGH(1)-125mg/kg, GGH(1)-250mg/kg and GGH(1)-500mg/kg treated mice had significantly lower body weight gain and feeding efficiency ratio. Consistent with the effects on body weight gain, GGH(1)-125mg/kg, GGH(1)-250mg/kg and GGH(1)-500mg/kg decreased the weights of visceral adipose tissues. GGH(1)-125mg/kg, GGH(1)-250mg/kg and GGH(1)-500mg/kg significantly decreased plasma levels of triglyceride. Consistent with the effects on feeding efficiency ratio, GGH(1)-125mg/kg, GGH(1)-250mg/kg and GGH(1)-500mg/kg decreased plasma leptin concentrations. Plasma AST and ALT were in the physiological range and organs were not different following GGH(1) treatment compared with obese controls, indicating that GGH(1) does not show any toxic effects on liver. These results suggest that GGH(1) reduces obesity by regulating appetite and visceral lipid metabolism in C57BL/6N mice. Of the 3 GGH(1) concentrations, GGH(1)-500mg/kg seems to be most effective in improving obesity and visceral lipid disorders.